[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-381992-105":59,"doc-detail-381992-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","telomeres-dysfunction-maintenance-aging-and-cancer","Telomeres: Dysfunction, Maintenance, Aging and Cancer","","Aging drives major scientific focus due to mounting social and economic burdens from the aging global population. Aging is characterized by multiple molecular and cellular processes that interact to shape aging outcomes. From telomere biology, this review examines how telomere dysfunction may amplify or accelerate core molecular and biochemical mechanisms and contribute to age-associated illnesses such as cancer and neurodegeneration. It also highlights newly identified mechanistic actions of telomere maintenance, informing therapeutic and preventive strategies.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/telomeres-dysfunction-maintenance-aging-and-cancer/381992/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/telomeres-dysfunction-maintenance-aging-and-cancer/381992.png","ImageObject",300,407,{"name":92,"@type":93},"kopisore","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-24","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What roles do telomeres and telomere-capping proteins play in preventing DNA damage recognition?","Question",{"text":112,"@type":113},"Telomeres are terminal chromosome elements bound by proteins that control their activities and prevent being recognized as DNA damage. When telomeres shorten critically, they lose adequate capping ability and exposed ends trigger DDR.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does telomere dysfunction relate to cellular senescence?",{"text":117,"@type":113},"Telomere dysfunction initiates telomere-associated DDR foci (TIFs/TAFs), supporting the development of cellular senescence. DDR signaling restrains proliferation and contributes to irreversible arrest linked to organismal aging and age-related diseases.",{"name":119,"@type":110,"acceptedAnswer":120},"What is the senescence-associated secretory phenotype (SASP), and how can it propagate senescence?",{"text":121,"@type":113},"SASP is a secretory program from senescent cells comprising proinflammatory cytokines. It drives chronic systemic inflammation and can alter the extracellular matrix, affect stem cell activity, encourage transdifferentiation, and spread the senescent phenotype to neighboring cells.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},381992,1790415974,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":52,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},962090880963,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","Volume 15, Number 6; 2595-2631, December 2024  \n[http://dx.doi.org/10.14336/AD.2023.1128](http://dx.doi.org/10.14336/AD.2023.1128)  \nReview  \nTelomeres: Dysfunction, Maintenance, Aging and Cancer  \nPan Liao1,2,3\\#, Bo Yan2,3\\#, Conglin Wang2,3\\#, Ping Lei1,2,3*  \n1The School of Medicine, Nankai University, Tianjin, China. 2Haihe Laboratory of Cell Ecosystem, Department of Geriatrics, Tianjin Medical University General Hospital, Tianjin, China. 3Tianjin Geriatrics Institute, Tianjin Medical University General Hospital, Tianjin, China.  \n[Received October 17, 2023; Revised November 26, 2023; Accepted November 28, 2023]  \nABSTRACT: Aging has emerged at the forefront of scientific research due to the growing social and economic costs associated with the growing aging global population. The defining features of aging involve a variety of molecular processes and cellular systems, which are interconnected and collaboratively contribute to the aging process. Herein, we analyze how telomere dysfunction potentially amplifies or accelerates the molecular and biochemical mechanisms underpinning each feature of aging and contributes to the emergence of age-associated illnesses, including cancer and neurodegeneration, via the perspective of telomere biology. Furthermore, the recently identified novel mechanistic actions for telomere maintenance offer a fresh viewpoint and approach to the management of telomeres and associated disorders. Telomeres and the defining features of aging are intimately related, which has implications for therapeutic and preventive approaches to slow aging and reduce the prevalence of age-related disorders.  \nKey words: telomere dysfunction, TBDs, maintenance mechanisms, age-related disorders, therapeutic, aging hallmarks  \nTelomeres are genetic elements found at the terminal positions of linear chromosomes. The TTAGGG repeats that make up telomeric DNA in vertebrates are bound by a group of proteins responsible for controlling their biological activities and preventing them from being recognized as DNA damage. Such recognition can trigger a DNA damage response (DDR), leading to telomere– telomere fusion and genetic instability. The unavailability of telomerase, an RNA-dependent DNA polymerase and reverse transcriptase, renders standard DNA polymerases inefficient in accomplishing complete replication of linear DNA templates. Additionally, due to nucleolytic processing, DNA replication produces chromosomes with progressively shorter telomeres [1] . The phenomenon of telomeres reaching a critical length causes them to lose their ability to bind adequate telomere-capping proteins and become detectable as exposed DNA ends [2] . This event then stimulates DDR pathways, leading to increased expression levels of the cell cycle inhibitors p16 and p21, which in turn restrain proliferation [3,4] . Despite being  \nshortened, these telomeres still maintain an adequate number of telomere-binding proteins to prevent fusion and block DNA repair [5–8] . This process fuels a continuous DNA damage signal, conferring an unalterable arrest in proliferative activities. Eventually, this triggers and preserves cellular senescence, which is a major factor associated with organismal aging and several age-related diseases [9,10] . Initiation of the DDR at telomeres, referred to as tDDR, yields the creation of telomere dysfunction-induced DNA damage foci (TIFs) or telomere-associated DDR foci (TAFs), which are indicators of cellular senescence in both cultured cells and tissues (Table 1) . Apoptotic [11,12] or autophagic [13] cell death may occur in some types of cells due to telomere dysfunction.  \nCellular senescence is hallmarked by alterations in cellular structures, organelles, gene expression, and chromatin, along with irreversible cell cycle arrest [14] . Notably, the senescence-associated secretory phenotype (SASP), produced by senescent cells, is a complex  \ncollection of proinflammatory cytokines. This results in chronic systemic ","cbCaijdqHUWcoO7c","https://ap.wps.com/l/cbCaijdqHUWcoO7c","pdf",1718241,37,"English","# Review: Telomeres: Dysfunction, Maintenance, Aging and Cancer\n## Abstract\n## Telomere dysfunction and DDR (tDDR) in cellular senescence\n## SASP and chronic inflammation mechanisms\n## Table 1: Comparisons of TL measurement methods","[{\"question\":\"What roles do telomeres and telomere-capping proteins play in preventing DNA damage recognition?\",\"answer\":\"Telomeres are terminal chromosome elements bound by proteins that control their activities and prevent being recognized as DNA damage. When telomeres shorten critically, they lose adequate capping ability and exposed ends trigger DDR.\"},{\"question\":\"How does telomere dysfunction relate to cellular senescence?\",\"answer\":\"Telomere dysfunction initiates telomere-associated DDR foci (TIFs/TAFs), supporting the development of cellular senescence. DDR signaling restrains proliferation and contributes to irreversible arrest linked to organismal aging and age-related diseases.\"},{\"question\":\"What is the senescence-associated secretory phenotype (SASP), and how can it propagate senescence?\",\"answer\":\"SASP is a secretory program from senescent cells comprising proinflammatory cytokines. It drives chronic systemic inflammation and can alter the extracellular matrix, affect stem cell activity, encourage transdifferentiation, and spread the senescent phenotype to neighboring cells.\"}]","Telomeres: Dysfunction, Maintenance, Aging and Cancer | PDF",1790248392,93]